Journal
CELL REPORTS
Volume 30, Issue 13, Pages 4386-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.03.018
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Funding
- BIOASTER investment
- French government (Agence Nationale pour la Recherche, France [ANR]) through the programme d'Investissement d'Avenir [ANR-10-AIRT-03]
- University Hospital of Toulouse
- Delegation Regionale a la Recherche Clinique des Hopitaux de Toulouse, France [NCT01990716]
- Fondation pour la Recherche Medicale, France (FRM) [ECO20170637477]
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Colonic macrophages are considered to be major effectors of inflammatory bowel diseases (IBDs) and the control of gut inflammation through C-type lectin receptors is an emerging concept. We show that during colitis, the loss of dectin-1 on myeloid cells prevents intestinal inflammation, while the lack of mannose receptor (MR) exacerbates it. A marked increase in dectin-1 expression in dextran sulfate sodium (DSS)-exposed MR-deficient mice supports the critical contribution of dectin-1 to colitis outcome. Dectin-1 is crucial for Ly6C(high)CCR2(high) monocyte population enrichment in the blood and their recruitment to inflamed colon as precursors of inflammatory macrophages. Dectin-1 also promotes inflammasome-dependent interleukin-1 beta (IL-1 beta) secretion through leukotriene B4 production. Interestingly, colonic inflammation is associated with a concomitant overexpression of dectin-1/CCL2/LTA4H and downregulation of MR on macrophages from IBD patients. Thus, MR and dectin-1 on macrophages are important mucosal inflammatory regulators that contribute to the intestinal inflammation.
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